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Titolo:
ISOFORM TRANSITIONS OF THE MYOSIN BINDING-PROTEIN-C FAMILY IN DEVELOPING HUMAN AND MOUSE MUSCLES - LACK OF ISOFORM TRANSCOMPLEMENTATION IN CARDIAC-MUSCLE
Autore:
GAUTEL M; FURST DO; COCCO A; SCHIAFFINO S;
Indirizzi:
EUROPEAN MOL BIOL LAB,MEIERHOFSTR 1 D-69117 HEIDELBERG GERMANY UNIV POTSDAM,DEPT CELL BIOL POTSDAM GERMANY UNIV PADUA,DEPT BIOMED SCI,CNR,CTR MUSCLE BIOL & PHYSIOPATHOL I-35100PADUA ITALY
Titolo Testata:
Circulation research
fascicolo: 1, volume: 82, anno: 1998,
pagine: 124 - 129
SICI:
0009-7330(1998)82:1<124:ITOTMB>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHICKEN SKELETAL-MUSCLE; MYBP-C; HYPERTROPHIC CARDIOMYOPATHY; IMMUNOELECTRON MICROSCOPY; MONOCLONAL-ANTIBODIES; TROPONIN-T; TITIN; GENE; EXPRESSION; PHOSPHORYLATION;
Keywords:
FAMILIAL HYPERTROPHIC CARDIOMYOPATHY; MYOSIN BINDING PROTEIN C; C-PROTEIN ISOFORMS; EMBRYONIC EXPRESSION PATTERNS; CARDIAC MUSCLE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
39
Recensione:
Indirizzi per estratti:
Citazione:
M. Gautel et al., "ISOFORM TRANSITIONS OF THE MYOSIN BINDING-PROTEIN-C FAMILY IN DEVELOPING HUMAN AND MOUSE MUSCLES - LACK OF ISOFORM TRANSCOMPLEMENTATION IN CARDIAC-MUSCLE", Circulation research, 82(1), 1998, pp. 124-129

Abstract

Mutations in the gene for the cardiac isoform of myosin binding protein C (MyBP-C) have been identified as the cause of chromosome 11-associated autosomal-dominant familial hypertrophic cardiomyopathy (FHC). Most mutations produce a truncated polypeptide that lacks the sarcomeric binding region. We have now investigated the expression pattern of the cardiac and skeletal isoforms of cMyBP-C in mice and humans by in situ hybridization and immunofluorescence microscopy using specific antibodies and probes. We demonstrate that the cardiac isoform is expressed only in cardiac muscle throughout development. The slow and fast isoforms of MyBP-C remain specific for skeletal muscle, where they can be coexpressed. Immunological evidence also suggests that an embryonic isoform of MyBP-C precedes the expression of slow MyBP-C in developingskeletal muscle. This suggests that transcomplementation of MyBP-C isoforms is possible in skeletal but not cardiac muscle.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 22:20:35